Abstract

Skeletal muscle is a plastic tissue and one of the responses to various physiological and pathological conditions is changes in protein synthesis or degradation rate. Various anabolic stimuli lead to muscle hypertrophy, while inactivity, denervation, spinal cord section, and other disuse conditions cause skeletal muscle atrophy. Today, skeletal muscles are considered as an endocrine organ and have important functions such as power production, movement, and breathing as well as glycemic control, metabolic homeostasis and regulation of metabolic genes. Therefore, loss of muscle mass affects homeostasis and leads to insulin resistance, type 2 diabetes, and obesity and results in increased morbidity and mortality. While the major anabolic pathway regulating protein synthesis in skeletal muscle is IGF1-PI3K-Akt-mTOR signaling pathway, the myostatin-Smad2/3 pathway plays a major role in the suppression of protein synthesis. On the other hand, the ATP-dependent ubiquitin-proteasome system, the cytosolic calcium-dependent calpain system, and lysosomal proteases play an important role in muscle atrophy. The pathways that control protein synthesis and degradation work in a coordinated fashion. Elucidating the molecular mechanisms playing role in controlling protein balance in skeletal muscle is of crucial importance to develop therapies and rehabilitation strategies for preservation of muscle tissue function.